动物实验证实厚朴酚及和厚朴酚具有防治急慢性抑郁作用,其主要机制是抗氧化和抗炎:通过直接清除自由基以及提高机体的核因子E2相关因子-2抗氧化信号通路和抗氧化酶活性间接清除自由基而抑制活性氧生成;通过阻滞磷脂酰肌醇-3蛋白激酶/蛋白激酶B,细胞外信号调节激酶/丝裂原活化蛋白激酶和把关受体/丝裂原活化蛋白激酶信号通路抑制炎性细胞因子表达和小胶质细胞、星形细胞的激活,保护脑神经。也可增强脑内5-羟色胺能神经功能,提高脑源性神经营养因子表达,促进海马神经再生,产生抗抑郁作用;还可下调抑郁时的下丘脑-垂体-肾上腺轴功能的亢进,改善抑郁样行为。

In animal experiments magnolol and honokiol have the pharmacologic effects in prevention and treatment for acute and chronic depression. Their basic mechanisms are antioxidation and anti-inflammation: by scavenging direct free radial and eliminating indirect free radial through up-regulating Nrf2 anti-oxidative signaling pathway and activity of antioxidases to decrease produce of ROS, and by blocking these signaling pathways of PI3K/Akt, ERK/MAPK and TLR/MAPK to inhibit the expression of inflammatory cytokines, and activation of microgliocyte and astrocyte, and to produce neuroprotective effect in brain. Magnolol and honokiol improve function of 5-hydroxytryptaminergic nerve, and expression of brain-derived neurotrophic factor, and neurogenesis of hippocampus, to produce antidepressant-like effects. Magnolol and honokiol ameliorate depressant-like behaviors by downregulating function of hypothalamus-hypophysis-adrenal axis.

R285.5；R964